Capsular polysaccharide synthesis, cell division and radiation sensitivity are controlled by the capR (lon) gene, as well as other genes in E. coli K-12. The overall objectives of the proposed research are: (a) to understand the mechanisms of control of cell division at a molecular level as related to mutations in E. coli K-12 designated capR, sulA and sulB. The capR mutation causes sensitivity to UV, X-rays, ozone and furadantin (a radiomimetic drug). After treatment with UV, capR mutants for nonseptate filaments that do not divide and will not produce a clone. Either mutation in sulA or sulB reverses the sensitivity of capR mutants to UV and furadantin. CapR sulA, and sulB map in different regions of the E. coli K-12 chromosome. (b) to understand how capR mutations also control, at the molecular level, synthesis of the enzymes of polysaccharide synthesis and overproduction of the capsular polysaccharide (with emphasis on the galETK operon). (c) to understand how our recently cloned genes specifying a major outer membrane protein and two other polypeptides (none of which are the capR gene product) control capsular polysaccharide synthesis in capR mutants. We have cloned the capR ion gene and identified and purified to homogeneity the capR ion gene specified protein (94 Kd monomer). It is a DNA-binding protein and also an ATP-dependent protease that is inhibited by DNA. It also has DNA-stimulated and casein-stimulated ATPase activities. It bind better to UV-irradiated DNA than to unirradiated DNA. We are studying the protein and its functions as well as seeking normal E. coli proteins that are proteolyzed (either activated or inactivated) by this unique enzyme.